Journal
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
Volume 71, Issue 1, Pages 2-14Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/NEN.0b013e31823cc7a6
Keywords
beta-amyloid; Alzheimer disease; Amygdala; Cerebellum; Cerebral cortex; Cholinesterases; Hippocampus; Olfactory structures; Thioflavin-S
Categories
Funding
- Canadian Institutes of Health Research [MOP-82798]
- Canadian Institutes of Health Research Vascular Health and Dementia Initiative [DOV-78344]
- Capital Health Research Fund
- Nova Scotia Health Research Foundation
- Faculty of Medicine of Dalhousie University
- Multiple Sclerosis Society of Canada
- National Institutes of Neurological Disorders and Stroke [NS057429]
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Histochemical analysis of Alzheimer disease (AD) brain tissues indicates that butyrylcholinesterase (BuChE) is present in beta-amyloid (A beta) plaques. The role of BuChE in AD pathology is unknown, but an animal model developing similar BuChE-associated A beta plaques could provide insights. The APP(SWE)/PSEN1dE9 transgenic mouse (ADTg), which develops A beta plaques, was examined to determine if BuChE associates with these plaques, as in AD. We found that in mature ADTg mice, BuChE activity associated with A beta plaques. The A beta-, thioflavin-S- and BuChE-positive plaques mainly accumulated in the olfactory structures, cerebral cortex, hippocampal formation, amygdala, and cerebellum. No plaques were stained for acetylcholinesterase activity. The distribution and abundance of plaque staining in ADTg closely resembled many aspects of plaque staining in AD. Butyrylcholinesterase staining consistently showed fewer plaques than were detected with A beta immunostaining but a greater number of plaques than were visualized with thioflavin-S. Double-labeling experiments demonstrated that all BuChE-positive plaques were A beta positive, whereas only some BuChE-positive plaques were thioflavin-S positive. These observations suggest that BuChE is associated with a subpopulation of A beta plaques and may play a role in AD plaque maturation. A further study of this animal model could clarify the role of BuChE in AD pathology.
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